| Summary: | Janus kinases (JAKs) are a family of cytosolic tyrosine kinases that regulate cytokine signal
transduction, including cytokines involved in a range of inflammatory diseases, such as
rheumatoid arthritis, psoriasis, atopic dermatitis, and inflammatory bowel disease. Several
small-molecule JAK inhibitors (JAKis) are now approved for the treatment of various
immune-mediated inflammatory diseases. There are, however, key differences between
these agents that could potentially translate into unique clinical profiles. Each JAKi has a
unique chemical structure, resulting in a distinctive mode of binding within the catalytic cleft
of the target JAK, and giving rise to distinct pharmacological characteristics. In addition, the
available agents have differing selectivity for JAK isoforms, as well as off-target effects
against non-JAKs. Other differences include effects on haematological parameters, DNA
damage repair, reproductive toxicity, and metabolism/elimination. Here we review the
pharmacological profiles of the JAK inhibitors abrocitinib, baricitinib, filgotinib, peficitinib,
tofacitinib, and upadacitinib.
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